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F Ivars

Publications and source records attributed to F Ivars.

30 records · Page 2Linked to original sources
PubMed1984

The immune response to bacterial dextrans. IV. Antibody idiotypes.

Anti-idiotypic antisera (a-Id) were prepared in SJL mice against the dextran B512 (Dex)-specific hybridoma antibody D.16.6 (mu, kappa) of C57BL/6 origin. Such a-Id were specific for the D.16.6 antibody, but the idiotypic determinants recognized were not hapten modifiable. The a-Id were used in radioimmunoassays (RIA) to study the genetic control of the expression of the D.16.6 idiotype (Id) in a variety of mouse strains. It was found that all mouse strains tested expressed this Id as a component of the normal background immunoglobulin (Ig) in their sera. Only in mice of the IgCHb haplotype, however, was the Id found in association with Dex-specific antibodies. Furthermore, even in IgCHb mouse strains, not all individuals expressed Id-positive anti-Dex antibodies. Because the D.16.6 Id is a "recurrent" natural Id, but a "non-dominant" Id in the Dex response of IgCHb mouse strains, these observations contradict our previous suggestions on the selection of "dominant" Id from the pool of "naturally" produced Ig.

Animals↗
PubMed1983

Immune response to bacterial dextrans. II. T cell control of antibody isotypes.

The isotype distribution of Dextran B 512 (Dex)-specific plaque-forming cells (PFC) and serum antibodies was studied after in vivo immunization in C57BL/6 mice. Although IgG2b and IgG3 could also be detected in most individuals, the majority of non-IgM PFC were of the IgA isotype. All classes other than IgM were T cell-dependent, as shown by their complete absence in athymic "nude" mice. This unusual isotype pattern was further investigated by studying the antibody responses to the same Dex epitope coupled to a protein carrier, and to a different hapten coupled to the carrier Dex or to a protein. The results show that IgA responses are epitope-related and selectively associated with anti-Dex antibodies: no IgA PFC are detected against a hapten coupled to Dex or proteins, while the enhanced levels of helper cell reactivity provided by protein carrier to Dex result in the appearance of IgG1 antibodies in addition to IgA. These results indicate that T cells that modulate isotype patterns in these responses can discriminate between Dex- and DNP-specific B cells in the response to the same carrier. Since the same idiotype is detected on a large fraction of the IgM and IgA anti-Dex response and antiidiotypic helper cells have previously been detected in normal C57BL/6 mice, we suggest that idiotype-specific T cells control the production of IgA antibodies upon immunization with Dex.

Animals↗
PubMed1983

An example of major histocompatibility complex-linked control of idiotypic interactions.

Normal euthymic mice, injected i.v. with low doses of syngeneic monoclonal antibodies carrying "recurrent" idiotypes, develop a specific increase in numbers of splenic IgM plaque-forming cells that are paratopically and idiotypically similar to the injected antibody. We have now studied the responsiveness to a C57BL/6 anti-dextran a(1 leads to 6) and BALB/c anti-TNP (trinitrophenyl) monoclonal antibodies in a variety of strains. It was found that such responses are controlled by two linkage groups, namely major histocompatibility complex (MHC) and Ig-1.

Animals↗
PubMed1983

The immune response to bacterial dextrans. I. Genetic control of responsiveness.

The in vivo antibody response to the thymus-independent (TI) antigen dextran B512 (Dex) was studied in various mouse strains. We found no non-responder strains but rather that the magnitude of Dex-specific plaque-forming cell and serum antibody responses varied markedly among individual mice, even if these were of the same age and litter and kept in the same environment. This was the case both for mouse strains previously described genetically as high (IgCHb,j) and for those described as low (IgCHa) responders to Dex [14]. In 'low'-responder BALB/c mice, the responsiveness to Dex increased with age, such that a large fraction of these mice responded as well as 'high'-responder C57BL/6 mice. Analysis of aged back-cross populations derived from IgCHb and IgCHa parental strains further substantiated these findings. Thus, all backcross mice, irrespective of IgCH haplotype, responded on the average equally well to Dex. According to our studies, therefore, the assignation of high or low responsiveness to IgCH locus-linked genes cannot be done unequivocally.

Aging↗
PubMed1982

Antigen-independent, IgM-induced antibody responses: requirement for "recurrent" idiotypes.

Anti-idiotypic antibodies (a-Id) were produced in syngeneic mice against two monoclonal IgM antibodies of BALB/c origin, TNP. 11 and SP/603. In plaque inhibition tests, using IgM-secreting hybridoma cells and anti-idiotypic antibodies, these two IgM proteins, as well as the anti-TNP myeloma protein MOPC 460 (IgA) were found to carry non-cross-reactive idiotypes. Analysis of the anti-trinitrophenyl (TNP) plaque-forming cells (PFC) in BALB/c mice, either normal or immunized with TNP-horse red blood cells, revealed that in addition to the MOPC 460 Id, also the SP/603 Id is recurrent and expressed by a fraction of the anti-TNP antibody-secreting cells in all individuals tested. In contrast, the TNP. 11 Id could not be detected in any BALB/c mouse studied. TNP. 11 and SP/603 antibodies were then characterized by their ability to induce an antigen-independent anti-TNP response in normal BALB/c mice. While TNP. 11 was found to be inactive, the same titers of SP/603 IgM induced antigen-specific PFC all of which expressed the SP/603 Id, and increased titers of circulating IgM molecules carrying the same Id, suggesting that "recurrent" but not "nonrecurrent" Id are competent in this respect. A fraction of these SP/603-induced, SP/603-positive anti-TNP antibodies also carried MOPC 460 Id, suggesting expression on the same molecule of idiotypic determinants found on independent non-cross-reactive "recurrent" idiotypes.

Animals↗
PubMed1982

Idiotypic characterization of antibody-induced antibody responses.

Anti-idiotypic antisera were produced in syngeneic (C57BL/6) mice against a monoclonal anti-Dextran B512 (Dex) antibody (38-13). In radioimmunoassays, anti-idiotypic antibodies were shown to react with the homologous idiotype, while failing to recognize another monoclonal anti-Dex antibody, independently derived from C57BL/6 mice (D-16). Plaque inhibition tests confirmed the specificity of the anti-idiotypic antibodies and revealed that the 38-13 idiotype is expressed by about half of all anti-Dex antibodies produced in C57BL/6, but not in CBA mice. Injection of normal (but not athymic) C57BL/6 mice with low doses of 38-13 monoclonal antibodies, contained culture supernatants or ascitic fluids, resulted in a 10-20 fold increase in the numbers of anti-Dex PFC detected in the spleen 5 days later, the majority of which carried the 38-13 idiotype.

Animals↗
PubMed1981

Regulation of T cell growth factor production: arrest of TCGF production after 18 hours in normal lectin-stimulated mouse spleen cell cultures.

The detailed kinetics of TCGF accumulation in Con A-stimulated spleen cell cultures shows a maximum at 24 hr, with a subsequent decrease in activity. This decrease is not due to the appearance of inhibitory substances "masking" TCGF activity. Pulse experiments show that the rate of TCGF production falls sharply after 18 hr and is completely arrested after 24 hr of Con A stimulation. The arrest in TCGF production is the result neither of culture depletion in medium components nor of limiting accessory cell function or inactivation of the lectin, and it thus seem to be the result of inactivation of TCGF-producing T cells. This regulation is not the result of a TCGF-mediated feedback mechanism but rather of lectin-induced suppressive cells that appear in culture after 24 hr and turn off de novo production of TCGF in fresh cultures.

Animals↗
PubMedDate not supplied

From the mechanisms of lymphocyte activation to internal activity in the immune system.

The principles of lymphocyte activation were summarized for all three sets of immunocompetent cells: B cells, cytotoxic cells and helper T lymphocytes. They were then used to derive the basic mechanisms and specificities which drive internal activity in the normal immune system and which select available antibody repertoires. It was postulated that "natural antibodies" are induced by "natural helper cells" and are selected on the basis of their idiotypic profiles, which are complementary to available T-helper-cell repertoires. "Natural idiotypes" would then carry idiotopes similar to MHC epitopes, the predominant germ-line specificity of T-cell repertoires.

Animals↗
PubMedDate not supplied

Anti-Ia.7 antibodies recognize a "major" idiotype of the anti-TNP antibody response in BALB/c mice.

Monoclonal antibodies to Ia.7 were used, in parallel with other antibodies specific for "major" and "private" idiotopes, to define idiotypic profiles in the primary anti-trinitrophenyl plaque forming cell (PFC) response of BALB/c and C57BL/6 mice. A considerable fraction (25%) of BALB/c but not C57BL/6 PFC were inhibited by anti-Ia.7 antibodies, which failed to inhibit PFC with other paratopic specificities. These results suggest idiotypic mimicry between "major" antibody clonotypes and MHC determinants which might play a role in the selection of antibody repertoires.

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